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Atrial fibrillation (AF) is the most common arrhythmia requiring treatment. The adverse outcomes commonly attributed to AF include symptomatic palpitations, dyspnea and exertional intolerance, and increased risk of thromboembolic complications, especially stroke. Because of the morbidity of this condition, several different treatment strategies have been derived to improve patient outcome. One of the strategies that are being used increasingly is catheter ablation. Presently, this is an aggressive, extensive ablation procedure designed to isolate triggering foci from electric conduction to the body of the atria and modifying atrial substrate to disrupt or prevent conduction/propagation of reentrant wave fronts. This procedure can be of long duration and associated with extensive myocardial destruction. Most of the ablation is performed in the systemic circulation. Because of these factors, systemic embolic events, especially stroke, have always been feared complications associated with this procedure.1 Although the prevalence of stroke complications has been low, concern has been raised in recent years about the observation of asymptomatic cerebral embolism (ACE) on diffusion-weighted MRI.2–4

Article see p 835

ACE lesions after catheter ablation of AF were first reported by Lickfett et al5 and since have been described by several groups. The mechanisms leading to the formation of ACE lesions have not been completely elucidated but are presumed to be because of microembolism to the small terminal intracerebral arteries.1 The components of the microembolic material causing ACE lesions after AF catheter ablation are hypothesized to be thrombus, gas microbubbles, heat-denatured albumin microbubbles, thermal coagulum, and avulsed tissue.6 Because this procedure does not involve catheter manipulation in the aortic root or aortic valve, dislodged calcium and cholesterol plaque probably do not have a role in ACE lesion production as …